Plasma proteomic signature of the risk of developing mobility disability: A 9‐year follow‐up
Introduction Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data‐driven discovery phase investigation to identify plasma proteins tha...
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| Vydané v: | Aging cell Ročník 19; číslo 4; s. e13132 - n/a |
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| Hlavní autori: | , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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England
John Wiley & Sons, Inc
01.04.2020
John Wiley and Sons Inc |
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| ISSN: | 1474-9718, 1474-9726, 1474-9726 |
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| Abstract | Introduction
Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data‐driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community‐dwelling older adults without mobility disability at baseline.
Methods
We investigated 660 women and men, aged 71.9 ± 6.0 (60–94) years, who participated in the Invecchiare in Chianti, “Aging in the Chianti Area” study and completed the 400‐m walk at fast pace (400‐m walk) at enrollment. Median follow‐up time was 8.57 [interquartile, 3.20–9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400‐m walk. Protein‐specific Cox proportional hazard model was adjusted for sex, age, and other important covariates.
Results
Plasma levels of 75 proteins predicted mobility disability (p < .05). Significant proteins were enriched for the KEGG “PI3K‐Akt signaling,” “phagosomes,” and “cytokine–cytokine receptor interaction” pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin‐2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility.
Conclusion
CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community‐dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability.
Among 1,301 plasma proteins assessed, cathepsin S, thrombospondin‐2, and growth/differentiation factor 15 significantly and independently predicted mobility loss in 660 community‐dwelling adults. Proteins associated with mobility loss were enriched for senescence‐associated secretory phenotype and for proteins in the PI3K‐Akt, phagosome, or cytokine–cytokine receptor interaction pathways. High plasma levels of SASP‐induced proteins related to inflammation and phagocytes activation mark a condition of high risk of mobility loss. |
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| AbstractList | Introduction: Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data-driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community-dwelling older adults without mobility disability at baseline. Methods: We investigated 660 women and men, aged 71.9 ± 6.0 (60-94) years, who participated in the Invecchiare in Chianti, "Aging in the Chianti Area" study and completed the 400-m walk at fast pace (400-m walk) at enrollment. Median follow-up time was 8.57 [interquartile, 3.20-9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400-m walk. Protein-specific Cox proportional hazard model was adjusted for sex, age, and other important covariates. Results: Plasma levels of 75 proteins predicted mobility disability (p <.05). Significant proteins were enriched for the KEGG "PI3K-Akt signaling," "phagosomes," and "cytokine-cytokine receptor interaction" pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin-2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility. Conclusion: CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community-dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability. Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data-driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community-dwelling older adults without mobility disability at baseline.INTRODUCTIONMobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data-driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community-dwelling older adults without mobility disability at baseline.We investigated 660 women and men, aged 71.9 ± 6.0 (60-94) years, who participated in the Invecchiare in Chianti, "Aging in the Chianti Area" study and completed the 400-m walk at fast pace (400-m walk) at enrollment. Median follow-up time was 8.57 [interquartile, 3.20-9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400-m walk. Protein-specific Cox proportional hazard model was adjusted for sex, age, and other important covariates.METHODSWe investigated 660 women and men, aged 71.9 ± 6.0 (60-94) years, who participated in the Invecchiare in Chianti, "Aging in the Chianti Area" study and completed the 400-m walk at fast pace (400-m walk) at enrollment. Median follow-up time was 8.57 [interquartile, 3.20-9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400-m walk. Protein-specific Cox proportional hazard model was adjusted for sex, age, and other important covariates.Plasma levels of 75 proteins predicted mobility disability (p < .05). Significant proteins were enriched for the KEGG "PI3K-Akt signaling," "phagosomes," and "cytokine-cytokine receptor interaction" pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin-2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility.RESULTSPlasma levels of 75 proteins predicted mobility disability (p < .05). Significant proteins were enriched for the KEGG "PI3K-Akt signaling," "phagosomes," and "cytokine-cytokine receptor interaction" pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin-2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility.CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community-dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability.CONCLUSIONCTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community-dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability. Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data-driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community-dwelling older adults without mobility disability at baseline. We investigated 660 women and men, aged 71.9 ± 6.0 (60-94) years, who participated in the Invecchiare in Chianti, "Aging in the Chianti Area" study and completed the 400-m walk at fast pace (400-m walk) at enrollment. Median follow-up time was 8.57 [interquartile, 3.20-9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400-m walk. Protein-specific Cox proportional hazard model was adjusted for sex, age, and other important covariates. Plasma levels of 75 proteins predicted mobility disability (p <.05). Significant proteins were enriched for the KEGG "PI3K-Akt signaling," "phagosomes," and "cytokine-cytokine receptor interaction" pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin-2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility. CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community-dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability. IntroductionMobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data‐driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community‐dwelling older adults without mobility disability at baseline.MethodsWe investigated 660 women and men, aged 71.9 ± 6.0 (60–94) years, who participated in the Invecchiare in Chianti, “Aging in the Chianti Area” study and completed the 400‐m walk at fast pace (400‐m walk) at enrollment. Median follow‐up time was 8.57 [interquartile, 3.20–9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400‐m walk. Protein‐specific Cox proportional hazard model was adjusted for sex, age, and other important covariates.ResultsPlasma levels of 75 proteins predicted mobility disability (p < .05). Significant proteins were enriched for the KEGG “PI3K‐Akt signaling,” “phagosomes,” and “cytokine–cytokine receptor interaction” pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin‐2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility.ConclusionCTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community‐dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability. Introduction Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data‐driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community‐dwelling older adults without mobility disability at baseline. Methods We investigated 660 women and men, aged 71.9 ± 6.0 (60–94) years, who participated in the Invecchiare in Chianti, “Aging in the Chianti Area” study and completed the 400‐m walk at fast pace (400‐m walk) at enrollment. Median follow‐up time was 8.57 [interquartile, 3.20–9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400‐m walk. Protein‐specific Cox proportional hazard model was adjusted for sex, age, and other important covariates. Results Plasma levels of 75 proteins predicted mobility disability (p < .05). Significant proteins were enriched for the KEGG “PI3K‐Akt signaling,” “phagosomes,” and “cytokine–cytokine receptor interaction” pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin‐2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility. Conclusion CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community‐dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability. Among 1,301 plasma proteins assessed, cathepsin S, thrombospondin‐2, and growth/differentiation factor 15 significantly and independently predicted mobility loss in 660 community‐dwelling adults. Proteins associated with mobility loss were enriched for senescence‐associated secretory phenotype and for proteins in the PI3K‐Akt, phagosome, or cytokine–cytokine receptor interaction pathways. High plasma levels of SASP‐induced proteins related to inflammation and phagocytes activation mark a condition of high risk of mobility loss. Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of mobility disability remains unknown. This study conducted a data-driven discovery phase investigation to identify plasma proteins that predict the incidence of mobility disability in community-dwelling older adults without mobility disability at baseline. We investigated 660 women and men, aged 71.9 ± 6.0 (60-94) years, who participated in the Invecchiare in Chianti, "Aging in the Chianti Area" study and completed the 400-m walk at fast pace (400-m walk) at enrollment. Median follow-up time was 8.57 [interquartile, 3.20-9.08] years. SOMAscan technology was used to measure 1,301 plasma proteins at enrollment. The incident of mobility disability was defined as inability to complete the 400-m walk. Protein-specific Cox proportional hazard model was adjusted for sex, age, and other important covariates. Plasma levels of 75 proteins predicted mobility disability (p < .05). Significant proteins were enriched for the KEGG "PI3K-Akt signaling," "phagosomes," and "cytokine-cytokine receptor interaction" pathways. After multiple comparison adjustment, plasma cathepsin S (CTSS; hazard ratio [HR] 1.33, 95% CI: 1.17, 1.51, q = 0.007), growth/differentiation factor 15 (GDF15; HR: 1.45, 95% CI: 1.23, 1.72, q = 0.007), and thrombospondin-2 (THBS2; HR: 1.44, 95% CI: 1.22, 1.69, q = 0.007) remained significantly associated with high risk of losing mobility. CTSS, GDF15, and THBS2 are novel blood biomarkers associated with new mobility disability in community-dwelling individuals. Overall, our analysis suggests that cellular senescence and inflammation should be targeted for prevention of mobility disability. Among 1,301 plasma proteins assessed, cathepsin S, thrombospondin‐2, and growth/differentiation factor 15 significantly and independently predicted mobility loss in 660 community‐dwelling adults. Proteins associated with mobility loss were enriched for senescence‐associated secretory phenotype and for proteins in the PI3K‐Akt, phagosome, or cytokine–cytokine receptor interaction pathways. High plasma levels of SASP‐induced proteins related to inflammation and phagocytes activation mark a condition of high risk of mobility loss. |
| Audience | Academic |
| Author | Fantoni, Giovanna Tanaka, Toshiko Bandinelli, Stefania Semba, Richard D. Osawa, Yusuke Candia, Julián Ferrucci, Luigi Biancotto, Angélique |
| AuthorAffiliation | 3 Clinical Research Core National Institute on Aging National Institutes of Health Baltimore MD USA 4 Laboratory of Human Carcinogenesis Center for Cancer Research National Cancer Institute NIH Bethesda MD USA 6 Geriatric Unit Azienda Sanitaria di Firenze Florence Italy 1 Longitudinal Study Section Translational Gerontology Branch National Institute on Aging National Institutes of Health Baltimore MD USA 5 Precision Immunology, Immunology and Inflammation Research Therapeutic Area Sanofi Cambridge MA USA 2 Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD USA |
| AuthorAffiliation_xml | – name: 5 Precision Immunology, Immunology and Inflammation Research Therapeutic Area Sanofi Cambridge MA USA – name: 1 Longitudinal Study Section Translational Gerontology Branch National Institute on Aging National Institutes of Health Baltimore MD USA – name: 2 Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD USA – name: 3 Clinical Research Core National Institute on Aging National Institutes of Health Baltimore MD USA – name: 4 Laboratory of Human Carcinogenesis Center for Cancer Research National Cancer Institute NIH Bethesda MD USA – name: 6 Geriatric Unit Azienda Sanitaria di Firenze Florence Italy |
| Author_xml | – sequence: 1 givenname: Yusuke orcidid: 0000-0002-7706-5166 surname: Osawa fullname: Osawa, Yusuke email: yusuke.osawa@nih.gov organization: National Institutes of Health – sequence: 2 givenname: Richard D. surname: Semba fullname: Semba, Richard D. organization: Johns Hopkins University School of Medicine – sequence: 3 givenname: Giovanna surname: Fantoni fullname: Fantoni, Giovanna organization: National Institutes of Health – sequence: 4 givenname: Julián surname: Candia fullname: Candia, Julián organization: NIH – sequence: 5 givenname: Angélique surname: Biancotto fullname: Biancotto, Angélique organization: Sanofi – sequence: 6 givenname: Toshiko surname: Tanaka fullname: Tanaka, Toshiko organization: National Institutes of Health – sequence: 7 givenname: Stefania surname: Bandinelli fullname: Bandinelli, Stefania organization: Azienda Sanitaria di Firenze – sequence: 8 givenname: Luigi surname: Ferrucci fullname: Ferrucci, Luigi email: FerrucciLu@grc.nia.nih.gov organization: National Institutes of Health |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32157804$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.5334/jors.166 10.1111/j.1532-5415.2000.tb03873.x 10.1371/journal.pone.0026332 10.1038/srep46362 10.1021/pr800545q 10.1002/stem.2120 10.1161/01.RES.0000202804.84885.d0 10.1016/j.bbrc.2016.08.138 10.1038/s41598-017-14755-5 10.1016/j.ab.2015.03.003 10.1101/gad.1874010 10.1038/gene.2012.27 10.1007/s11357-018-0042-y 10.1111/jgs.14742 10.3389/fphys.2018.01712 10.1096/fj.06-7924com 10.1016/j.cels.2016.02.015 10.1111/acel.12799 10.1177/1535370216672747 10.1001/jama.2011.1246 10.1161/hq1201.098945 10.1111/imm.12042 10.1016/j.matbio.2017.12.012 10.1074/jbc.M116.719054 10.1161/CIRCRESAHA.118.312816 10.1073/pnas.96.26.14888 10.1038/s41569-018-0064-2 10.3389/fimmu.2018.01593 10.1074/mcp.M111.014340 10.1161/01.RES.0000141019.20332.3e 10.1016/j.bbapap.2011.10.002 10.1093/gerona/56.10.M644 10.3390/ijms18071540 10.1001/jama.295.17.2018 10.3233/CBM-181940 10.1042/CS20150605 10.1371/journal.pone.0137924 10.2105/AJPH.2011.300631 10.1093/geronb/55.1.S41 10.1038/s41569-018-0002-3 |
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| Copyright | 2020 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd. 2020 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. COPYRIGHT 2020 John Wiley & Sons, Inc. 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| References_xml | – volume: 56 start-page: M644 issue: 10 year: 2001 end-page: 649 article-title: Measuring higher level physical function in well‐functioning older adults: Expanding familiar approaches in the Health ABC study publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 18 issue: 7 year: 2017 article-title: Thrombospondins: A role in cardiovascular disease publication-title: International Journal of Molecular Sciences – volume: 291 start-page: 9920 issue: 19 year: 2016 end-page: 9928 article-title: Cathepsin S contributes to the pathogenesis of muscular dystrophy in mice publication-title: Journal of Biological Chemistry – volume: 7 start-page: 46362 year: 2017 article-title: Myostatin mediates abdominal aortic atherosclerosis progression by inducing vascular smooth muscle cell dysfunction and monocyte recruitment publication-title: Scientific Reports – volume: 21 start-page: 2004 issue: 12 year: 2001 end-page: 2010 article-title: Tumor necrosis factor receptor superfamily 14 is involved in atherogenesis by inducing proinflammatory cytokines and matrix metalloproteinases publication-title: Arteriosclerosis, Thrombosis, and Vascular Biology – volume: 13 start-page: 515 issue: 7 year: 2012 end-page: 522 article-title: Variation in FCN1 affects biosynthesis of ficolin‐1 and is associated with outcome of systemic inflammation publication-title: Genes and Immunity – volume: 6 issue: 10 year: 2011 article-title: From SOMAmer‐based biomarker discovery to diagnostic and clinical applications: A SOMAmer‐based, streamlined multiplex proteomic assay publication-title: PLoS ONE – volume: 5 year: 2017 article-title: Web tool for navigating and plotting SomaLogic ADAT Files publication-title: Journal of Open Research Software – volume: 9 start-page: 1712 year: 2018 article-title: GDF15 and growth control publication-title: Frontiers in Physiology – volume: 95 start-page: 515 issue: 5 year: 2004 end-page: 522 article-title: Thrombospondin‐2 is essential for myocardial matrix integrity: Increased expression identifies failure‐prone cardiac hypertrophy publication-title: Circulation Research – volume: 10 issue: 9 year: 2015 article-title: Lipocalin (LCN) 2 mediates pro‐atherosclerotic processes and is elevated in patients with coronary artery disease publication-title: PLoS ONE – volume: 18 start-page: 1 issue: 1 year: 2019 end-page: 26 article-title: A proteomic atlas of senescence‐associated secretomes for aging biomarker development publication-title: Plos Biology – volume: 11 issue: 6 year: 2012 article-title: Global stability of plasma proteomes for mass spectrometry‐based analyses publication-title: Molecular & Cellular Proteomics: MCP – volume: 478 start-page: 1528 issue: 4 year: 2016 end-page: 1533 article-title: Knockdown of FSTL1 inhibits oxLDL‐induced inflammation responses through the TLR4/MyD88/NF‐kappaB and MAPK pathway publication-title: Biochemical and Biophysical Research Communications – volume: 1824 start-page: 68 issue: 1 year: 2012 end-page: 88 article-title: Cysteine cathepsins: From structure, function and regulation to new frontiers publication-title: Biochimica Et Biophysica Acta – volume: 21 start-page: 3029 issue: 12 year: 2007 end-page: 3041 article-title: Cathepsin cysteine proteases in cardiovascular disease publication-title: The FASEB Journal – volume: 17 issue: 5 year: 2018 article-title: Plasma proteomic signature of age in healthy humans publication-title: Aging Cell – volume: 48 start-page: 1618 issue: 12 year: 2000 end-page: 1625 article-title: Subsystems contributing to the decline in ability to walk: Bridging the gap between epidemiology and geriatric practice in the InCHIANTI study publication-title: Journal of the American Geriatrics Society – volume: 55 start-page: S41 issue: 1 year: 2000 end-page: 50 article-title: Sex differences in the prevalence of mobility disability in old age: The dynamics of incidence, recovery, and mortality publication-title: Journals of Gerontology. Series B, Psychological Sciences and Social Sciences – year: 2019 article-title: Galectin‐8 in the onset of the immune response and inflammation publication-title: Glycobiology – volume: 123 start-page: 740 issue: 7 year: 2018 end-page: 744 article-title: Time and the metrics of aging publication-title: Circulation Research – volume: 478 start-page: 14 year: 2015 end-page: 22 article-title: Evaluating the effects of preanalytical variables on the stability of the human plasma proteome publication-title: Analytical Biochemistry – volume: 9 start-page: 1593 year: 2018 article-title: CD38 Is robustly induced in human macrophages and monocytes in inflammatory conditions publication-title: Frontiers in Immunology – volume: 138 start-page: 198 issue: 3 year: 2013 end-page: 207 article-title: Sialoadhesin ‐ a macrophage‐restricted marker of immunoregulation and inflammation publication-title: Immunology – volume: 65 start-page: 980 issue: 5 year: 2017 end-page: 988 article-title: Effect of physical activity on self‐reported disability in older adults: Results from the LIFE study publication-title: Journal of the American Geriatrics Society – volume: 68–69 start-page: 463 year: 2018 end-page: 473 article-title: Matrix metalloproteinases and liver fibrosis (translational aspects) publication-title: Matrix Biology – volume: 15 start-page: 505 issue: 9 year: 2018 end-page: 522 article-title: Inflammageing: Chronic inflammation in ageing, cardiovascular disease, and frailty publication-title: Nature Reviews Cardiology – volume: 33 start-page: 3291 issue: 11 year: 2015 end-page: 3303 article-title: Autocrine action of thrombospondin‐2 determines the chondrogenic differentiation potential and suppresses hypertrophic maturation of human umbilical cord blood‐derived mesenchymal stem cells publication-title: Stem Cells – volume: 15 start-page: 351 issue: 6 year: 2018 end-page: 370 article-title: Cysteine protease cathepsins in cardiovascular disease: From basic research to clinical trials publication-title: Nature Reviews Cardiology – volume: 7 start-page: 14248 issue: 1 year: 2017 article-title: Assessment of variability in the SOMAscan assay publication-title: Scientific Reports – volume: 24 start-page: 183 issue: 2 year: 2019 end-page: 193 article-title: Identification of biomarkers associated with progression and prognosis in bladder cancer via co‐expression analysis publication-title: Cancer Biomarkers – volume: 8 start-page: 113 issue: 1 year: 2009 end-page: 117 article-title: Standard operating procedures for serum and plasma collection: Early detection research network consensus statement standard operating procedure integration working group publication-title: Journal of Proteome Research – volume: 40 start-page: 419 issue: 5–6 year: 2018 end-page: 436 article-title: A framework for selection of blood‐based biomarkers for geroscience‐guided clinical trials: Report from the TAME Biomarkers Workgroup publication-title: Geroscience – year: 2019 article-title: Elevated plasma growth and differentiation factor‐15 is associated with slower gait speed and lower physical performance in healthy community‐dwelling adults publication-title: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences – volume: 24 start-page: 241 issue: 3 year: 2010 end-page: 255 article-title: IL‐4 induces cathepsin protease activity in tumor‐associated macrophages to promote cancer growth and invasion publication-title: Genes & Development – volume: 242 start-page: 250 issue: 3 year: 2017 end-page: 257 article-title: Secretory leukocyte protease inhibitor promising protective roles in obesity‐associated atherosclerosis publication-title: Experimental Biology and Medicine (Maywood) – volume: 2 start-page: 185 issue: 3 year: 2016 end-page: 195 article-title: Plasma proteome profiling to assess human health and disease publication-title: Cell Systems – volume: 306 start-page: 1113 issue: 10 year: 2011 end-page: 1121 article-title: Association between serum cathepsin S and mortality in older adults publication-title: JAMA – volume: 295 start-page: 2018 issue: 17 year: 2006 end-page: 2026 article-title: Association of long‐distance corridor walk performance with mortality, cardiovascular disease, mobility limitation, and disability publication-title: JAMA – volume: 102 start-page: 1508 issue: 8 year: 2012 end-page: 1515 article-title: Mobility and aging: New directions for public health action publication-title: American Journal of Public Health – volume: 98 start-page: 342 issue: 3 year: 2006 end-page: 350 article-title: GDF15/MIC‐1 functions as a protective and antihypertrophic factor released from the myocardium in association with SMAD protein activation publication-title: Circulation Research – volume: 129 start-page: 1077 issue: 12 year: 2015 end-page: 1081 article-title: Cyclic nucleotide phosphodiesterase 1 and vascular aging publication-title: Clinical Science (Lond) – volume: 96 start-page: 14888 issue: 26 year: 1999 end-page: 14893 article-title: Thrombospondin‐2: A potent endogenous inhibitor of tumor growth and angiogenesis publication-title: Proceedings of the National Academy of Sciences – ident: e_1_2_9_5_1 doi: 10.5334/jors.166 – ident: e_1_2_9_8_1 doi: 10.1111/j.1532-5415.2000.tb03873.x – ident: e_1_2_9_18_1 doi: 10.1371/journal.pone.0026332 – ident: e_1_2_9_40_1 doi: 10.1038/srep46362 – ident: e_1_2_9_38_1 doi: 10.1021/pr800545q – ident: e_1_2_9_15_1 doi: 10.1002/stem.2120 – ident: e_1_2_9_41_1 doi: 10.1161/01.RES.0000202804.84885.d0 – ident: e_1_2_9_13_1 doi: 10.1016/j.bbrc.2016.08.138 – ident: e_1_2_9_4_1 doi: 10.1038/s41598-017-14755-5 – ident: e_1_2_9_14_1 doi: 10.1016/j.ab.2015.03.003 – volume: 18 start-page: 1 issue: 1 year: 2019 ident: e_1_2_9_3_1 article-title: A proteomic atlas of senescence‐associated secretomes for aging biomarker development publication-title: Plos Biology – ident: e_1_2_9_12_1 doi: 10.1101/gad.1874010 – ident: e_1_2_9_24_1 doi: 10.1038/gene.2012.27 – ident: e_1_2_9_17_1 doi: 10.1007/s11357-018-0042-y – ident: e_1_2_9_23_1 doi: 10.1111/jgs.14742 – ident: e_1_2_9_7_1 doi: 10.3389/fphys.2018.01712 – ident: e_1_2_9_22_1 doi: 10.1096/fj.06-7924com – ident: e_1_2_9_11_1 doi: 10.1016/j.cels.2016.02.015 – ident: e_1_2_9_35_1 doi: 10.1111/acel.12799 – ident: e_1_2_9_43_1 doi: 10.1177/1535370216672747 – ident: e_1_2_9_16_1 doi: 10.1001/jama.2011.1246 – ident: e_1_2_9_19_1 doi: 10.1161/hq1201.098945 – ident: e_1_2_9_27_1 doi: 10.1111/imm.12042 – ident: e_1_2_9_28_1 doi: 10.1016/j.matbio.2017.12.012 – ident: e_1_2_9_36_1 doi: 10.1074/jbc.M116.719054 – ident: e_1_2_9_10_1 doi: 10.1161/CIRCRESAHA.118.312816 – ident: e_1_2_9_34_1 doi: 10.1073/pnas.96.26.14888 – ident: e_1_2_9_9_1 doi: 10.1038/s41569-018-0064-2 – ident: e_1_2_9_2_1 doi: 10.3389/fimmu.2018.01593 – ident: e_1_2_9_44_1 doi: 10.1074/mcp.M111.014340 – ident: e_1_2_9_30_1 doi: 10.1161/01.RES.0000141019.20332.3e – ident: e_1_2_9_39_1 doi: 10.1016/j.bbapap.2011.10.002 – ident: e_1_2_9_33_1 doi: 10.1093/gerona/56.10.M644 – year: 2019 ident: e_1_2_9_37_1 article-title: Galectin‐8 in the onset of the immune response and inflammation publication-title: Glycobiology – ident: e_1_2_9_6_1 doi: 10.3390/ijms18071540 – ident: e_1_2_9_25_1 doi: 10.1001/jama.295.17.2018 – ident: e_1_2_9_32_1 doi: 10.3233/CBM-181940 – ident: e_1_2_9_42_1 doi: 10.1042/CS20150605 – ident: e_1_2_9_26_1 doi: 10.1371/journal.pone.0137924 – ident: e_1_2_9_29_1 doi: 10.2105/AJPH.2011.300631 – ident: e_1_2_9_20_1 doi: 10.1093/geronb/55.1.S41 – ident: e_1_2_9_21_1 doi: 10.1038/s41569-018-0002-3 – year: 2019 ident: e_1_2_9_31_1 article-title: Elevated plasma growth and differentiation factor‐15 is associated with slower gait speed and lower physical performance in healthy community‐dwelling adults publication-title: Journals of Gerontology. 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Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the... Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the development of... Introduction: Mobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the... IntroductionMobility disability is a powerful indicator of poor health in older adults. The biological and pathophysiological mechanism underlying the... Among 1,301 plasma proteins assessed, cathepsin S, thrombospondin‐2, and growth/differentiation factor 15 significantly and independently predicted mobility... |
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| SubjectTerms | 1-Phosphatidylinositol 3-kinase Aged Aged, 80 and over Aging AKT protein Biomarkers - blood Blood proteins Cathepsin S Cathepsins - blood Cytokines Disabled Persons - psychology Female Follow-Up Studies Growth Differentiation Factor 15 - blood growth/differentiation factor 15 Humans Middle Aged Mobility mobility disability Older people Original Phagosomes Plasma Plasma levels Plasma proteins Proteins Proteomics Risk Factors Senescence Thrombospondin Thrombospondins - blood thrombospondin‐2 Walking - psychology |
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| Title | Plasma proteomic signature of the risk of developing mobility disability: A 9‐year follow‐up |
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